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Paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Acyanotic vs cyanotic congenital heart disease?

A

Cyanotic - when O2 rich and O2 poor blood mixes = less O2 rich blood to tissues = cyanosis.
Acyanotic - defect doesn’t normally interfere w the amount of O2 in the blood that reaches tissues.

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2
Q

What are the cyanotic heart defects?

A
  • Tetralogy of Fallot
  • Transposition of the great vessels
  • Pulmonary atresia
  • Total anomalous pulm venous return
  • Hypoplastic left heart syndrome
  • Tricuspid valve anomalies
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3
Q

What are the acyanotic heart defects?

A
  • Atrial septal defect
  • Ventricular septal defect
  • Atrioventricular septal defect
  • Patent ductus arteriosus
  • Pulm valve stenosis
  • Aortic valve stenosis
  • Coarctation of the aorta
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4
Q

What are the fetal shunts?

A
  1. Foramen ovale - shunt between RA and LA -> blood skips RV and pulm circ and lungs
  2. Ductus venosus - shunt between umbilical vein and IVC, blood skips the liver
  3. Ductus arteriosus - shunt between pulmonary artery and aorta, blood skips the lungs
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5
Q

When do the shunts shut and how?

A

First breath expands the alveoli = decreased pulm vascular resistance = fall in pressure in RA = LA pressure > RA pressure = foramen ovale closes, over next few weeks is sealed shut = fossa ovalis.
Prostaglandins keep ductus arteriosus open, increased O2 in blood = reduced prostaglandins so it closes and becomes ligamentum arteriosum.
Ductus venosus stops functioning because the umbilical cord is clamps and there is no flow in umbilical veins, closes and becomes ligamentum venosum.

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6
Q

Draw out the fetal circulatory system with the shunts

A

Answer on iPad

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7
Q

What are the features of innocent murmurs? What are they?

A
  • Short
  • Soft
  • Systolic
  • Symptomless
  • Situation dependent - esp if gets quieter w standing or only when child has a fever or is anaemic
    Innocent murmurs in common in children, caused by fast blood flow through various areas of the heart in systole.
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8
Q

What are the features of a murmur that are concerning and require further ix?

A
  • Loud
  • Diastolic
  • Louder on standing
  • Failure to thrive, feeding difficulty, cyanosis, SOB
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9
Q

What are the ix into murmurs?

A
  • ECG
  • CXR - to see if cardiomegaly
  • Transthoracic echo using doppler
  • Cardiac MRI or CT (avoid in children due to radiation)
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10
Q

What are the different types of atrial septal defect?

A
  1. Ostium secondum - septum secondum fails to full close = hole
  2. Patent foramen ovale - foramen ovale fails to close
  3. Ostium primum - septum primum fails to fully close = hole, leads to atrioventricular valve defects and is more of a atrioventricular septal defect
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11
Q

What are complications of ASD?

A
  • Stroke: DVT -> embolus -> brain instead of PE
  • AF or atrial flutter
  • Pulm HTN and R sided HF
  • Eisenmenger syndrome
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12
Q

How do ASD cause R sided HF?

A

Higher pressure in the LA than the RA so blood flows though defect from LA to RA = right ventricle dilation = right sided HF and pulm HTN due to increased blood in pulm circ.
Get an ejection systolic murmur due to increased flow across the pulm valve because of the shunt.

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13
Q

What is the presentation of ASDs?

A
  • Mid systolic crescendo decrescendo murmur, loudest at upper L sternal border w fixed split second heart sound
  • Often asymptomatic in childhood and present in adulthood w dyspnoea, HF and stroke
  • Childhood sx - SOB, difficulty feeding, poor weight gain, recurrent LRTIs
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14
Q

What is a split heart sound?

A

Can hear the closure of the aortic and pulm valves at different times, can be normal w inspiration but a fixed split is always the same in inspiration and expiration.
Happens because the RV has more blood to empty before the pulm valve can close.

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15
Q

What is the management of ASDs?

A
  • Small and asymptomatic ASD - watch and wait
  • Transvenous catheter closure or open heart surgery (central stenotomy) to correct ASD if problematic
  • Anticoags used to reduce risk of clots in stroke and adults
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16
Q

What are ECG findings in ASD?

A
  • Tall P wave = right atrial enlargement
  • Right bundle branch block
  • Right axis deviation
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17
Q

What is the presentation of a VSD?

A
  • Antenatal scan or murmur in newborn baby check
  • Poor feeding
  • Dyspnoea and tachypnoea
  • Failure to thrive
  • Asymptomatic
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18
Q

What is the murmur in VSD?

A

Pan systolic in L lower sternal border in 3rd and 4th ICS. Can have systolic thrill.

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19
Q

What are the consequences of having a VSD?

A
  1. Left to right shunt -> acyanotic but causes R sided overload, RHF and pulm HTN
  2. If pulm HTN continues the pressure in the R side > L = right to left shunt = cyanotic = Eisenmenger syndrome
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20
Q

What is the management of VSD?

A
  • Small VSD without pulm HTN or HF = watch and wait, often close spont
  • Surgical correction = transvenous catheter closure or stenotomy via open heart surgery, for large VSDs w HR normally between 3-6m
  • HF = diuretics, captopril, need increased calories
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21
Q

What is a complication of VSD?

A

Infective endocarditis = increased risk, abx prophylaxis during surgical procedures should be considered

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22
Q

What are the CF of large VSD?

A
  • HF w SOB and faltering growth after 1w old
  • Recurrent chest infections
  • Tachypnoea, tachy, enlarged liver from HF
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23
Q

What is PDA?

A

Patent ductus arteriosus - should close in first few weeks of life, unclear why happens:
RF - genetic, maternal infection eg. rubella, prematurity

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24
Q

How does PDA cause problems?

A

Left to right shunt = pulm HTN and R sided heart overload = RV hypertrophy. Increased blood flows through pulm circ and into L side of heart = LV hypertrophy.

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25
Q

What is the presentation of a PDA?

A
  • Murmur - cont crescendo decrescendo murmur, can cover up second heart sound, often under L clavicle, machinery murmur
  • SOB
  • Difficulty feeding
  • Poor weight gain
  • LRTIs
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26
Q

What are the ix into PDA? How is it managed?

A

Ix - echo
Manage - monitor until 1 year w echo, if still present after 1 year it is unlikely will close spont and will have surgical closure.
Can also use indomethacin ? will block prostaglandins and close the hole ?

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27
Q

What is the nitrogen washout test?

A

Used to see if heart disease in a cyanosed neonate:
- Placed in 100% O2 box or ventilator for 10 mins
- If R radial PaO2 from ABG is low can diagnose cyanotic congenital heart disease if have excluded lung disease and pulm HTN
- If PaO2 is high = not cyanotic heart disease

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28
Q

What is the management of a blue baby?

A

AtoE - may need mechanical ventilation
Start prostaglandin E infusion to maintain ductus arteriosus patency, cyanotic babies are often duct dependent, the blood flows from the aorta into the pulm arteries where it is oxygenated at the lungs, if there was no patent ductus arteriosus the blood would never reach the lungs, due to the R to L shunt

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29
Q

What is Eisenmenger syndrome?

A

Is a consequence of acyanotic congenital heart disease - L to R shunt in ASD, VSD and PDA causes increased pressure in the R side of the heart due to increased blood flow, so the shunt changes direction R to L = Eisenmenger syndrome.
Can develop after 1-2 years w large shunts or in adulthood w small shunts. Pregnancy can speed developing it up so women w hx of small shunt need echo and close monitoring.

30
Q

What are the examination findings associated w pulm HTN?

A
  • RV heave - bigger contraction against increased pressure in the lungs
  • Loud P2 - loud second heart sound due to forceful shutting of pulm valve
  • Raised JVP
  • Peripheral oedema
31
Q

What are the examination findings related to underlying septal defect? Murmurs

A

ASD - mid systolic crescendo decrescendo murmur loudest at upper L sternal border
VSD - pan systolic murmur loudest at L lower sternal border
PDA - cont crescendo decrescendo machinery

32
Q

What are the examination findings related to R to L shunt and chronic hypoxia?

A
  • Cyanosis
  • Clubbing
  • Dyspnoea
  • Plethoric complexion
33
Q

What is the prognosis of Eisenmenger syndrome?

A

Life expectancy reduced by 20 years
Cause of death - HF, infection, VTE, haemorrhage
50% mortality in pregnancy

34
Q

What is the management of Eisenmenger syndrome?

A
  • Surgical correction of underlying defect to prevent development of Eisenmenger syndrome
  • Eisenmenger syndrome isn’t reversible, only definitive treatment is a heart lung transplant
  • Pum HTN - sildenafil
  • Polycythaemia - venesection
  • VTE prophylaxis w anticoags
  • Prophylactic abx to prevent IE
35
Q

What are the cardinal anatomical features of ToF?

A
  1. Large VSD
  2. Overriding aorta
  3. Pulmonary valve stenosis
  4. RV hypertrophy
36
Q

What is the normal anatomy of the aortic valve? What is different in stenosis?

A

Aortic valve opens to allow blood to flow from LV into the aorta but closes to prevent blood flowing back into the LV, the valve has 3 leaflets normally. In stenosis the aortic valve is narrow and restricts blood flow from LV into aorta. No of leaflets is abnormal.

37
Q

What is the presentation of aortic stenosis?

A
  • Asymptomatic murmur
  • Fatigue, SOB
  • Reduced exercise tolerance
  • Chest pain on exertion, syncope
  • Critical aortic stenosis - HF w/i few months of birth
38
Q

What are the signs of aortic stenosis?

A
  • Ejection systolic murmur loudest at the aortic area, radiates to carotids and is crescendo decresecendo
  • Carotid thrill
  • Small vol slow rising pulse
  • Ejection click
39
Q

What is the management of aortic stenosis?

A
  • Echo to assess diagnosis
  • Worsens over time so need reg follow up w echos, ECGs and exercise testing - this will help decide when to intervene
  • Treatment - percutaneous balloon aortic valvoplasty, surgical aortic valvotomy, valve replacement eventually
40
Q

How is aortic stenosis severity graded?

A

> 40 = severe

41
Q

What are the complications of valve stenosis?

A
  • HF
  • Ventricular arrhythmia
  • Bacterial endocarditis
  • Sudden death, often on exertion
  • LV outflow tract obstruction in aortic stenosis
42
Q

What is the normal anatomy of the pulm valve? And what happens when is it stenosed?

A

Normally 3 leaflets, lets blood flow from RV into the pulm artery. In stenosis the leaflets are thickened or fused.

43
Q

What are the CF of pulm stenosis?

A
  • Most asymptomatic
  • Severe pulm stenosis - fatigue on exertion, SOB, dizzy, fainting
44
Q

What are the signs of pulm stenosis?

A
  • Ejection systolic murmur loudest at pulm area
  • Palpable pulm thrill
  • RV heave due to RV hypertrophy
  • Raised JVP
45
Q

What is the management of pulm stenosis?

A
  • Watch and wait
  • Balloon valvuloplasty via venous catheter treatment of choice
46
Q

What is coarctation of the aorta?

A

When the duct closes, the aorta also constricts. Narrowing (coarctation) of the aortic arch, usually around the ductus arteriosus. The narrowing reduces the pressure of blood flowing to the arteries that are distal to the narrowing and increases pressure in the areas proximal to the narrowing eg. heart.

47
Q

What is the presentation of coarctation of aorta?

A

Typical clinical picture - normal in first day of life and then acute circ collapse at about 2 days when duct closes.
Sick baby - severe HF - tachypnoea, poor feeding, grey and floppy

48
Q

What are the signs of coarctation of aorta?

A
  • Weak/absent femoral pulses
  • High BP in limbs supplied by arteries before the narrowing and low BP in limbs supplied by arteries after narrowing
  • Severe met acidosis
  • Systolic murmur below L clavicle
  • Underdevelopment of legs/Larm - reduced flow
49
Q

What is the management of coarctation of aorta?

A

Critical coarctation - prostaglandin E for patency of ductus arteriosus while wait for surgery - correct coarctation and ligate the ductus arteriosus.

50
Q

What is hypoplastic left heart syndrome?

A

Underdevelopment of the entire L side of the heart - small or absent mitral valve and aortic valve, small LV and ascending aorta, coarctation of aorta.

51
Q

What are the CF of hypoplastic L heart syndrome?

A

Antenatal detection w USS.
If present after birth = v v sick neonates, have duct dependent systemic circ, no flow through L side of heart = acidosis and rapid cardiovascular collapse, absence of all peripheral pulses.

52
Q

How do you manage hypoplastic L heart syndrome?

A

Norwood procedure then Glenn then Fontan - palliative surgery for congenital heart defects

53
Q

What is tetralogy of fallot?

A
  1. Ventricular septal defect
  2. Overriding aorta
  3. Pulm valve stenosis
  4. RV hypertrophy
54
Q

What are the consequences of tetralogy of fallot?

A

VSD = blood flow between ventricles
Overriding aorta = closer to the R side of the heart, right next to VSD = RV contracts and sends blood into the aorta, so more deoxygenated blood into the aorta
Pulm valve stenosis = greater resistance to blood flow, further encouraging blood into the aorta = R to L shunt = cyanosis
Increased strain on RV attempting to pump blood against resistance of LV = RV hypertrophy
BLOOD BYPASSES CHILDS LUNGS = CYANOSIS

55
Q

What are the RF of tetralogy of Fallot?

A
  • Rubella infection
  • Increased age
  • Alcohol consumption in pregnancy
  • Gestational diabetes
56
Q

What are the ix into tetralogy of Fallot?

A
  • Echo and doppler flow studies
  • CXR - boot shaped heart due to RV thickening
57
Q

What is the presentation of ToF?

A
  • Most cases picked up antenatally
  • Ejection systolic murmur by pulm stenosis on newborn baby check
  • Severe cases - HF before 1 year of age but can present later in older children in milder cases
58
Q

What are the signs of ToF?

A
  • Cyanosis
  • Clubbing
  • Poor feeding and weight gain
  • Ejection systolic murmur (pulm stenosis)
  • Tet spells
59
Q

What are Tet spells? Why are they dangerous?

A

Hypercyanotic spells - R to L shunt suddenly worsened = rapid increase in cyanosis, usually associated w irritability or inconsolable crying due to severe hypoxia and breathlessness, then pallor because of tissue acidosis.
Can lead to MI, cerebrovascular accidents or death if untreated.

60
Q

How might children react to hypercyanotic spells?

A

Children may squat or bring knees to their chest = increased systemic vascular resistance = blood in pulm vessels

61
Q

What is the medical management of hypercyanotic spells?

A
  • Supplementary O2
  • B blockers - relax the RV and increase flow into pulm vessels
  • IV fluids increase vol of blood flowing into pulm vessels
  • Morphine - decrease resp drive
  • Na bicarb - buffer met acidosis
  • Phenylephrine infusion increases systemic vascular resistance = increase flow in pulm vessels
62
Q

What is the management of tetralogy of Fallot?

A
  • Prostaglandins to maintain ductus arteriosus
  • Total surgical repair by open heart surgery is definitive, wait until ~6m but mortality about 5%
63
Q

What is transposition of the great arteries?

A

The attachments of the aorta and the pulm trunk are swapped - RV pumps blood into the aorta and the LV pumps blood into the pulm vessels. The two circulations don’t mix.
After birth the condition is immediately life threatening as the blood going to the body has no O2 = cyanosed.

64
Q

What is the presentation of transposition of the great arteries?

A
  • Antenatal USS often find defect
  • Cyanosis w/i first days of life
  • If have VSD or PDA this can compensate for a few days however a few weeks later = resp distress, tachy, poor feeding and weight gain
65
Q

What is the management of transposition of the great arteries?

A
  • Prostaglandin infusion to maintain ductus arteriosus will wait for more definitive treatment
  • Balloon septostomy to create a large atrial septal defect to allow circulation mixing
  • Open heart surgery = cardiopulm bypass machine to perform an arterial switch = definitive
66
Q

What is Ebstein’s anomaly?

A

Congenital heart condition where tricuspid valve is lower in the right side of the heart = bigger RA and smaller RV = reduced flow to pulm vessels.

67
Q

What is the presentation of Ebstein’s anomaly?

A
  • HF eg. oedema
  • Gallop rhythm and additional 3rd and 4th heart sounds
  • Cyanosis
  • SOB and tachypnoea
  • Poor feeding
  • Collapse or cardiac arrest
68
Q

What is the management of Ebstein’s anomaly?

A

Treat arrhythmias and heart failure, surgical correction and prophylactic abx can prevent IE.

69
Q

What are the differentials for pan systolic murmurs?

A
  • Mitral regurg
  • Tricuspid regurg
  • Ventricular septal defect at left lower sternal border
70
Q

What are the differentials for ejection systolic murmurs?

A
  • Aortic stenosis
  • Pulm stenosis
  • Hypertrophic obstructive cardiomyopathy
71
Q

What are the rules for murmurs ?

A

Above the nipple - ejection systolic eg. ASD
Below the nipple - pansystolic eg. VSD

Paediatrics (15 decks)

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